The aim of this research is to extend our understanding of host responses to ethylnitrosourea (ENU)-induced F-344 rat malignant gliomas in order to elucidate the role of immunity in the pathogenesis of human glial neoplasms and to explore the feasibility of immunotherapy against these tumors. Following transplacental induction of malignant astrocytic and mixed gliomas with ENU, transplantable derivatives of several of these autochthonous tumors have already been produced by direct animal and alternate culture to animal serial passage methods. This research deals with four early-vintage transplantable glioma lines, two of which are immunogenic and two which elicit tumor-stimulatory responses in immunized hosts. In vivo tumor rejection assays and Winn tumor neurtralization tests are employed: (a) to determine if these gliomas express individually-unique or cross-reactive tumor specific transplantation antigens and (b) to measure the extent to which rejection and stimulation responses are active when these tumors are grafted in the brain. BCG-priming/PPD-coupling combine non-specific and specific methods of immunizing animals against tumor grafts. Experiments are added to assess the potential of these methods in augmenting immunologically-mediated rejection or enhancement of gliomas implanted at either subcutaneous or intracerebral sites. Because the role of thymus-derived cells in mediating tumoricidal anti-glioma immunity or glioma growth-stimulatory processes has not been documented in vivo, investigations are planned to clarify T-effector and T-suppressor cell function in glioma immunity. Specifically, these studies include: first, tumor rejection assay in hosts rendered T-cell depleted by thymectomy; second, similar assays in chimeric animals reconstituted with thymus cells from tumor-bearing donors after treatment consisting of thymectomy/splenectomy/total-body irradiation; and third, Winn tests in which lymphoid elements, donated by glioma bearing hosts, are combined with glioma cells in vitro and then implanted in previously prepared glioma-immunized hosts.